• Yang Ruan, Shuai Meng, Ruofei Jia, Xiaojing Cao, and Zening Jin.
• Department of Cardiology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
• Am. J. Med. Sci. 2024 Jun 1; 367 (6): 397405397-405.

BackgroundNumerous studies have explored the therapeutic potential of microRNA (miR) in myocardial infarction (MI) treatment. This study focuses on the role of miR-322-5p in MI, particularly in its regulatory interaction with B-cell translocation gene 2 (BTG2).Materials And MethodsExpression levels of miR-322-5p and BTG2 were assessed in a rat MI model. Adenovirus altering miR-322-5p or BTG2 expression were administered to MI rats. Evaluation included cardiac function, inflammation, myocardial injury, pathological changes, apoptosis, and NF-κB pathway-related genes in MI rats post-targeted treatment. The miR-322-5p and BTG2 targeting relationship was investigated.ResultsMI rats exhibited low miR-322-5p and high BTG2 expression in the myocardial tissues. Restoration of miR-322-5p enhanced cardiac function, alleviated inflammation and myocardial injury, mitigated pathological changes and apoptosis, and deactivated the NF-κB pathway in MI rats. BTG2 expression was negatively-regulated by miR-322-5p. Overexpressed BTG2 counteracted miR-322-5p-induced cardioprotection on MI rats.ConclusionThis study provides evidence that miR-322-5p protects against MI by suppressing BTG2 expression.Copyright © 2024. Published by Elsevier Inc.

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